A study of the factors responsible for rate‐dependent shortening of the action potential in mammalian ventricular muscle.
A study of the factors responsible for rate‐dependent shortening of the action potential in mammalian ventricular muscle.
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对导致哺乳动物心室肌动作电位速率依赖性缩短的因素的研究。
DOI：
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发表时间：
1978
期刊：
影响因子：
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通讯作者：
B. R. Jewell
中科院分区：
文献类型：
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作者：
M. Boyett;B. R. Jewell
1.用细胞内微电极记录猫乳头肌等长收缩时浅层细胞的动作电位。有规律地刺激肌肉，并在规则(对照)反应之间的不同时间插入测试刺激。2.测试动作电位的持续时间(在80%复极时测量)随着测试刺激和前一刺激之间的间隔的增加而呈指数增加，并且通过数据绘制的曲线在测试间隔1.0%-1.5%S时达到平台期。这条曲线被认为反映了控制反应后膜电导恢复到刺激前的时间过程，被称为电恢复曲线。3.在较长的测试间期，动作电位时程再次增加，当刺激间隔为200-300 S时，动作电位时程接近静息状态值约0.5 S。4.在等长收缩中，增加刺激速率或浸泡钙离子浓度等干预措施，使电恢复曲线下移(动作电位时程缩短)和左移(刺激间期缩短)。曲线的这种变化伴随着其幅度的降低(即最早可能的动作电位和平台值之间的持续时间的差异)，但干预措施对电恢复时间进程的影响不同：刺激频率的增加会导致明显的减慢，而沐浴钙浓度的增加会使时间进程略有加快。5.刺激频率增加所引起的动作电位时程缩短可分为两部分，一部分是电恢复曲线下移所致，另一部分则取决于膜恢复连续反应之间的时间间隔。当刺激频率高于100min-1.6时，第二个成分变得越来越重要。在常规刺激静息准备和成对脉冲刺激所产生的张力阶梯期间，动作电位时程的变化也可以由电恢复曲线的下移和连续反应之间膜恢复程度的变化相互作用来解释。7.电恢复曲线的下移被认为是由于细胞内钙的积累和/或细胞外钾的积累，现有的证据被认为支持前一种机制。
1. An intracellular micro‐electrode was used to record action potentials from superficial cells of a cat papillary muscle during isometric contractions. The muscle was stimulated regularly and test stimuli were interpolated at various times between regular (control) responses. 2. The duration of test action potentials (measured at 80% repolarization) increases exponentially with time as the interval between the test stimulus and the preceeding stimulus is increased and a curve drawn through the data reaches a plateau at test intervals of 1.0‐1.5 s. This curve is considered to reflect the time course with which membrane conductances return to their pre‐stimulus values after a control response, and it is known as the 'electrical restitution curve'. 3. At much longer test intervals the action potential duration duration increases again and it approaches the rested state value of about 0.5 s when the interval between stimuli is 200‐300 s. 4. Interventions that raise the peak tension developed in isometric contractions, such as an increase in the rate of stimulation or in the bathing calcium concentration, displace the electrical restitution curve downwards (to shorter action potential durations) and to the left (to shorter stimulus intervals). This shift in the curve is accompanied by a reduction in its magnitude (i.e. the difference in duration between the earliest possible action potential and the plateau value), but the interventions differ in their effects on the time course of electrical restitution: an increase in stimulus frequency causes a marked slowing, whereas an increase in bathing calcium concentration produces a slight speeding up of its time course. 5. The reduction in action potential duration produced by an increase in stimulus frequency (rate‐dependent shortening) can be separated into two components, one resulting from the downward displacement of the electrical restitution curve and the other depending on the time available between consecutive responses for membrane recovery. The second component becomes increasingly important at stimulus frequencies above 100 min‐1. 6. Changes in action potential duration observed during the tension staircases produced by regular stimulation of a rested preparation and by paired pulse stimulation can also be accounted for by interaction of downward displacement of the electrical restitution curve and variations in the degree of recovery of the membrane between consecutive responses. 7. Downward displacement of the electrical restitution curve is thought to result from intracellular accumulation of calcium and/or extracellular accumulation of potassium, and the available evidence is considered to favour the former mechanism.